[Development of renal affection in obese patients]
Aim:
To characterize mechanisms, early markers and clinical signs of renal damage in obesity.
Material And Methods:
The trial covered 29 males aged under 50 years (mean age 37.7+/-9.3 years) with abdominal obesity having neither carbohydrate metabolism disturbances nor chronic renal disease. All the patients were examined for microalbuminuria (MAU), serum level of leptin. Radionuclide scintigraphy of the kidneys with an acute captopril test, tests for serum concentrations of endothelin-1, homocistein, uric acid, ultrasound dopplerography of the brachial artery for assessment of endothelium-related vasodilation (ERVD) were made in 24 patients. In 9 patients MAU and ERVD were estimated after 3 months of valsartan treatment (80 mg/day).
Results:
MAU was detected in 62% patients, its rate increasing with elevation of serum leptin and endothelin concentration. Under normal values of creatininemia and GFR, obese patients showed deletion of renal functional reserve (RFR). Patients with low RFR had maximal uricemia and homocysteinemia, serum endothelin-1. Such patients demonstrated also abnormal ERVD. 3-month valsartan intake led to elevation of ERVD and disappearance of MAU.
Conclusion:
Excessive leptin registered in obese patients provoked dysfunction of the endothelium of the intrarenal vessels manifesting with MAU, growth of endothelin-1 serum concentration and disorder of ERVD. This leads to unfavourable changes in filtrating function of the kidneys as seen from gradual deletion of RFR in the absence of hypercreatininemia. Elimination of MAU and ERVD disorders in obesity can be achieved by administration of angiotensin II receptor blockers.
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The kidneys are located in the retroperitoneal space on either side of the vertebral column, protected posteriorly by the 11th and 12th ribs. The right kidney sits slightly lower than the left owing to the presence of the liver...
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Obesity

